Benjamin D. Zeitlin

ORCID: 0000-0003-0110-0188
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About
Contact & Profiles
Research Areas
  • Angiogenesis and VEGF in Cancer
  • MRI in cancer diagnosis
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Nanoplatforms for cancer theranostics
  • Cell death mechanisms and regulation
  • Cancer, Hypoxia, and Metabolism
  • Periodontal Regeneration and Treatments
  • Cancer Mechanisms and Therapy
  • Mesenchymal stem cell research
  • Nanoparticle-Based Drug Delivery
  • RNA Interference and Gene Delivery
  • Kruppel-like factors research
  • Metal complexes synthesis and properties
  • Cell Adhesion Molecules Research
  • Trace Elements in Health
  • 3D Printing in Biomedical Research
  • Chemokine receptors and signaling
  • Extracellular vesicles in disease
  • Glioma Diagnosis and Treatment
  • Pharmacological Effects of Medicinal Plants
  • Synthesis of Organic Compounds
  • Innovative Teaching Methods
  • Phagocytosis and Immune Regulation
  • PI3K/AKT/mTOR signaling in cancer
  • Ferrocene Chemistry and Applications

University of the Pacific
2011-2023

University of Michigan
2005-2013

Michigan United
2013

Sylvester Comprehensive Cancer Center
2011

Angiogenesis Foundation
2006-2010

Michigan Center for Translational Pathology
2009

The University of Texas MD Anderson Cancer Center
2009

University of Strathclyde
2008

Argonne National Laboratory
2006

University of Chicago
2006

Abstract The current understanding of the interaction between endothelium and cancer cells is fundamentally based on concept that endothelial are responsive to differentiation survival signals originating from tumor cells. Whereas effect cell–secreted factors angiogenesis well established, little known about secreted by cell gene expression progression. Here, we show bcl-2 significantly higher in tumor-associated patients with head neck squamous carcinomas (HNSCC) as compared normal oral...

10.1158/0008-5472.can-07-1497 article EN Cancer Research 2007-10-15

Abstract Vascular endothelial growth factor (VEGF) induces expression of Bcl-2 in tumor-associated microvascular cells. We have previously reported that up-regulated cells is sufficient to enhance intratumoral angiogenesis and accelerate tumor growth. initially attributed these results Bcl-2–mediated cell survival. However, recent experiments, we observed conditioned medium from Bcl-2–transduced human dermal (HDMEC-Bcl-2) induce potent neovascularization the rat corneal assay, whereas empty...

10.1158/0008-5472.can-05-0140 article EN Cancer Research 2005-06-15

Inhibition of blood vessel formation is a viable therapeutic approach in angiogenesis-dependent diseases. We previously used combinatorial screening on vascular endothelial growth factor (VEGF)-activated cells to select the sequence CPQPRPLC and showed that motif Arg-Pro-Leu targets VEGF receptor-1 neuropilin-1. Here, we evaluated validated D (LPR), derivative molecule with strong antiangiogenesis attributes. This prototype drug markedly inhibits neovascularization three mouse models:...

10.1073/pnas.0915141107 article EN Proceedings of the National Academy of Sciences 2010-02-26

Abstract Bcl-2 is an antiapoptotic protein that up-regulated in several tumor types, and its expression levels have strong correlation to development of resistance therapy poor prognosis. We shown recently also functions as a proangiogenic signaling molecule activates nuclear factor-κB–mediated pathway resulting up-regulation the angiogenic chemokines CXCL1 CXCL8 by neovascular endothelial cells. Here, we evaluate antiangiogenic effect novel small-molecule inhibitor (TW37) developed using...

10.1158/0008-5472.can-05-3691 article EN Cancer Research 2006-09-01

Abstract Members of the Bcl-2 family play a major role in pathobiology head and neck cancer. We have shown that orchestrates cross talk between tumor cells endothelial direct effect on progression squamous cell carcinoma (HNSCC). Notably, is significantly up-regulated tumor-associated compared with normal oral mucosa patients HNSCC. Here, we evaluated TW-37, small-molecule inhibitor Bcl-2, cycle survival HNSCC xenografted tumors. TW-37 has an IC50 1.1 μmol/L for primary human averaged 0.3...

10.1158/1535-7163.mct-08-1078 article EN Molecular Cancer Therapeutics 2009-04-01

Recent evidence demonstrated that endothelial cells initiate signaling events enhance tumor cell survival, proliferation, invasion, and recurrence. Under this new paradigm for cellular crosstalk within the microenvironment, origin of may have a direct impact on pathobiology cancer. The purpose pilot study was to evaluate effect species (i.e. murine or human) xenograft growth response therapy. Tumor xenografts vascularized either with human microvascular were engineered, side-by-side,...

10.1371/journal.pone.0084236 article EN cc-by PLoS ONE 2013-12-31

10.1038/labinvest.2012.77 article EN publisher-specific-oa Laboratory Investigation 2012-05-07

Bcl-2 is an antiapoptotic protein that has also been found to function as a proangiogenic signaling molecule. Improvements in antiangiogenic therapy can be engendered by metronomic dosing. Thus, we hypothesized BH3-mimetic drugs antagonize family proteins may exert greater efficacy when dosed metronomically. To examine this hypothesis, employed AT101, orally available and well-tolerated drug established effective. In mouse xenograft model of human squamous cell carcinomas (SCC) includes...

10.1158/0008-5472.can-10-2873 article EN Cancer Research 2011-12-09

Nedel F, Soki FN, Conde MCM, Zeitlin BD, Tarquinio SBC, Nör JE, Seixas FK, Demarco FF. Comparative analysis of two colorimetric assays in dental pulp cell density. International Endodontic Journal, 44, 59–64, 2011. Aim To compare and contrast used for the measurement proliferation using types: stem cells (DPSC) human fibroblasts (HDPF). Methodology Dental or HDPF were seeded at 0.25 × 104 per well 96-well plates. Cell was evaluated after 24–72 h. At end experimental period, sulforhodamine B...

10.1111/j.1365-2591.2010.01796.x article EN International Endodontic Journal 2010-09-29

PURPOSE: Angiogenesis plays an important role in pancreas cancer pathobiology. Pancreatic tumor cells secrete vascular endothelial growth factor (VEGF), activating cell protein kinase C beta (PKCβ) that phosphorylates GSK3β to suppress apoptosis and promote proliferation microvessel formation. We used Enzastaurin (Enz) test the hypothesis inhibition of PKCβ results radiosensitization culture vivo. MATERIALS/METHODS: measured phosphorylation, VEGF pathway signaling, colony formation,...

10.1593/tlo.08151 article EN cc-by-nc-nd Translational Oncology 2008-12-01

Abstract Two genes are considered synthetic lethal if mutation of either alone allows cell viability, whereas simultaneous leads to death. A screen unveiled the dependency Wnt/β-catenin-addicted colorectal cancer cells on vascular endothelial growth factor receptor-1 kinase activity and suggested a novel therapeutic approach for this malignancy. (Clin Cancer Res 2009;15(24):7453–5)

10.1158/1078-0432.ccr-09-2578 article EN Clinical Cancer Research 2009-12-14

Tumors of the oral cavity are highly vascularized malignancies. Disruption neovascular networks was shown to limit access nutrients and oxygen tumor cells inhibit progression. Here, we evaluated effect activation an artificial death switch (iCaspase-9) expressed in endothelial on progression tumors. We used biodegradable scaffolds co-implant human dermal microvascular stably expressing iCaspase-9 (HDMEC-iCasp9) with cancer luciferase (OSCC3-luc or UM-SCC-17B-luc) immunodeficient mice....

10.1177/154405910608500508 article EN Journal of Dental Research 2006-05-01

Modeling the complex and prolonged development of mammalian central nervous system in vitro remains a profound challenge. Most studies human stem cell derived neurons are conducted over days to weeks may or not include glia. Here we have utilized single pluripotent line, TERA2.cl.SP12 derive both glial cells determined their differentiation functional maturation 1 year culture together with ability display epileptiform activity response pro-convulsant agents detect antiseizure drug actions....

10.3389/fnins.2023.1182720 article EN cc-by Frontiers in Neuroscience 2023-06-15
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